NEW INTERPRETATION OF SYSTOLIC-TIME INTERVALS FROM ACTIVE CROSS-BRIDGE MODEL

Using an active cross-bridge model proposed by the authors, it has bee n established theoretically that cross-bridge activation rate (K(a)) o f the left ventricular myocardium, which might correspond to the rate of binding of Ca2+ with troponin C, is approximately expressed as a si mple formula: K(a)=3/electromechanical systole (sec-1), although no de finitive biological proof has yet been provided for the equation. One hundred eighteen patients without significant cardiac disease and 6 pa tients who had atrioventricular block with a permanent pacemaker were evaluated to determine the K(a) value of the normal human left ventric ular myocardium (test 1), and to examine the effect of changes in hear t rate (test 2) as well as afterloading (test 3) or dobutamine infusio n (test 4) on K(a). The pacing rate was increased from 50 to 110 beats /min at 20-beat increments in test 2. Arterial pressure was elevated b y angiotensin 11 infusion in test 3, and 7 subjects received a continu ous dobutamine infusion in test 4. The K(a) value was found to be rela ted to heart rate, to be increased by dobutamine infusion, and to be d ecreased by myocardial lengthening due to afterloading. Dependence of K(a) on heart rate appeared to result from changes in myocardial lengt h. The K(a) value corrected for heart rate (K(ac)) had an average vari ation of only 4.6%, and was unrelated to age or myocardial length in i ndividual subjects. Thus, the K(ac) value of normal human left ventric ular myocardium appears to be nearly constant between individuals but to be increased by catecholamine infusion or myocardial shortening.